A common hypothesis, though not uncontroversial is that dopamine has a function of transmitting reward prediction error. According to this hypothesis, the phasic responses of dopamine neurons are observed when an unexpected reward is presented. These responses transfer to the onset of a conditioned stimulus after repeated pairings with the reward. Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to encode the prediction error of rewarding outcomes. In nature, we learn to repeat behaviors that lead to maximize rewards. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behavior. Temporal difference learning provides a computational model describing how the prediction error of dopamine neurons is used as a teaching signal.

Movement

Via the dopamine receptors D1, D2, D3, D4 and D5, dopamine reduces the influence of the indirect pathway, and increases the actions of the direct pathway within the basal ganglia. Insufficient dopamine biosynthesis in the dopaminergic neurons can cause Parkinson's disease, in which a person loses the ability to execute smooth, controlled movements.

Cognition and frontal cortex

In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder. It has been found that D1 receptors are responsible for the cognitive-enhancing effects of dopamine. On the converse, however, anti-psychoticmedications act as dopamine antagonists and are used in the treatment of positive symptoms in schizophrenia.

Regulating prolactin secretion

Dopamine is the primary neuroendocrine inhibitor of the secretion of prolactin from the anterior pituitary gland. Dopamine produced by neurons in the arcuate nucleus of the hypothalamus is secreted into the hypothalamo-hypophysial blood vessels of the median eminence, which supply the pituitary gland. The lactotrope cells that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion. Thus, in the context of regulating prolactin secretion, dopamine is occasionally called prolactin-inhibiting factor (PIF), prolactin-inhibiting hormone (PIH), or prolactostatin. Prolactin also seems to inhibit dopamine release, such as after orgasm, and is chiefly responsible for the refractory period.

Motivation and pleasure

Reinforcement

Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and ventral tegmental area) by naturally rewarding experiences such as food, sex, drugs, and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs such as cocaine, nicotine, and amphetamines, which seem to directly or indirectly lead to an increase of dopamine in these areas, and in relation to neurobiological theories of chemical addiction, arguing that these dopamine pathways are pathologically altered in addicted persons. Recent studies indicate that aggression may also stimulate the release of dopamine in this way.

Reuptake inhibition, expulsion

Cocaine and amphetamines inhibit the re-uptake of dopamine; however, they both influence separate mechanisms of action. Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150 percent) within the parameters of the dopamine neurotransmitters.

Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. By entering the presynaptic neuron, amphetamines force dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.

Incentive salience

Dopamine's role in experiencing pleasure has been questioned by several researchers. It has been argued that dopamine is more associated with anticipatory desire and motivation (commonly referred to as "wanting") as opposed to actual consummatory pleasure (commonly referred to as "liking"). Dopamine is not released when unpleasant or aversive stimuli are encountered, in effect enhancing the pleasure of avoidance or removal of the unpleasant stimuli.

Dopamine, learning, and reward-seeking behavior

Dopaminergic neurons of the midbrain are the main source of dopamine in the brain. Dopamine has been shown to be involved in the control of movements, the signaling of error in prediction of reward, motivation, and cognition. Cerebral dopamine depletion is the hallmark of Parkinson's disease. Other pathological states have also been associated with dopamine dysfunction, such as schizophrenia, autism, and attention deficit hyperactivity disorder in children, as well as drug abuse. Dopamine is closely associated with reward-seeking behaviors, such as approach, consumption, and addiction. Recent researches suggest that the firing of dopaminergic neurons is a motivational substance as a consequence of reward-anticipation. This hypothesis is based on the evidence that, when a reward is greater than expected, the firing of certain dopaminergic neurons increases, which consequently increases desire or motivation towards the reward.

Animal studies

Clues to dopamine's role in motivation, desire, and pleasure have come from studies performed on animals. In one such study, rats were depleted of dopamine by up to 99 percent in the nucleus accumbens and neostriatum using 6-hydroxydopamine.
With this large reduction in dopamine, the rats would no longer eat by their own volition. The researchers then force-fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to actually eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.

The effects of drugs that reduce dopamine levels in humans

In humans, however, drugs that reduce dopamine activity (neuroleptics, e.g. some antipsychotics) have been shown to reduce motivation, and to cause anhedonia a.k.a. the inability to experience pleasure.
Selective D2/D3 agonists pramipexole and ropinirole, used to treat Restless legs syndrome, have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale.
(The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)

Additionally, users of stimulants often have depleted dopamine levels after withdrawal from these addictive substances.

Opioid and cannabinoid transmission

Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability (liking).
This could explain why animals' "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.
Libido can be increased by drugs that affect dopamine, but not by drugs that affect opioid peptides or other neurotransmitters.

Sociability

Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hyperdopaminergic state in certain areas of the brain. In instances of bipolar disorder, manic subjects can become hypersocial, as well as hypersexual. This is also credited to an increase in dopamine, because mania can be reduced by dopamine-blocking anti-psychotics.

Processing of pain

Dopamine has been demonstrated to play a role in pain processing in multiple levels of the central nervous system including the spinal cord , periaqueductal gray (PAG), thalamus , basal gangliainsular cortex and cingulate cortex. Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in Parkinson's disease. Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome, fibromyalgia and restless legs syndrome. In general, the analgesic capacity of dopamine occurs as a result of dopamine D2 receptor activation; however, exceptions to this exist in the PAG, in which dopamine D1 receptor activation attenuates pain presumabley via activation of neurons involved in descending inhibition. In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.

Salience

Dopamine may also have a role in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things seeming more noticeable or important. This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.

One possible mechanism of paranoid thought architecture, both in schizophrenics and in amphetamine abusers (both groups are widely hypothesized to suffer from hyperabundance of dopamine), is as follows: hyperabundance of dopamine causes widespread salience: an impression of significance attendant to statements, events, things, etc. in the immediate environment. This heightened significance can frequently be disturbing since it may have no rational basis. The individual experiencing this heightened significance may attempt to account for it and in this way paranoid ideation begins as a theoretical structure designed to account for this disturbing impressionistic significance. On this model, the impression of heightened significance ("Meaning beyond meaning" or "things are not as they seem" as Carol North put it) is primary and gives rise to the theoretical efforts - the paranoid ideation. On this model, the paranoid ideation is engendered only indirectly by dopamine surfeit. If we follow this model, what is not clear, however, is the way in which exaggerated salience (supposing this to be a result of dopamine surfeit) gives rise to the sense of pervasive malfeasance which is a hallmark feature of paranoid schizophrenic and amphetamine-psychotic ideation. This sense of malfeasance need not be a direct product of salience; nor is it necessary that salience be a disquieting experience. It is neither a priori nor a posteriori true that salience leads inevitably to paranoid ideation. And the conviction of malfeasance may indeed have a non-sense-impressionistic source; i.e. there is no apparent reason (other than dogmatism) to follow the dictum that nothing is in the mind that was not first in the world of sense impressions. It may be that suspicion is engendered independently of impressions of salience. However, the two would seem philosophically linked in that it is hard to imagine an object of suspicion which is not also salient. The question then can be renewed: does the salience come first or the suspicion? It could be that they occur together but are distinct. In the case of paranoid ideation, it does not seem prima facie likely that this thought architecture would spring into existence simply because of salience. The sense of malefic conspiracy (a conspiracy which may be largely impersonal and theological, as in the case of Daniel Paul Schreber) is so consistent in paranoid ideation (of various kinds, in various individuals, of various origins) that it would seem to be a kind of mental capacity unto itself (albeit likely an exaggeration of this capacity, for vigilance or suspicion, e.g.), not something which is a product of a "suspicion-neutral" rational mind working to interpret irrational incidences of salience. That is, there is no reason to suppose that paranoid suspicion must be engendered by sense data of some kind (even of exaggerated salience) since this arbitrarily treats the suspicion as a learned response to certain sense data, rather than a capacity unto itself. (This would be analogous to treating human aggression as a learned response rather than as an innate capacity.) And indeed there would seem good reason to suppose the existence of an innate capacity for suspicion and vigilance, since these activities would tend toward individual survival.

Behavior disorders

Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug-taking behaviour may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.

Deficits in dopamine levels are implicated in attention-deficit hyperactivity disorder (ADHD), and stimulant medications used to successfully treat the disorder increase dopamine neurotransmitter levels, leading to decreased symptoms.

Links to psychosis

Abnormally high dopamine action has also been strongly linked to psychosis and schizophrenia,
Dopamine neurons in the mesolimbic pathway are particularly associated with these conditions. Evidence comes partly from the discovery of a class of drugs called the phenothiazines (which block D2dopamine receptors) that can reduce psychotic symptoms, and partly from the finding that drugs such as amphetamine and cocaine (which are known to greatly increase dopamine levels) can cause psychosis. Because of this, most modern antipsychotic medications, for example, Risperidone, are designed to block dopamine function to varying degrees.

High doses from 10 to 20 μg/kg/min is the "pressor" dose. This dose causes vasoconstriction, increases systemic vascular resistance, and increases blood pressure through α1 receptor activation; but can cause the vessels in the kidneys to constrict to the point where they will become non-functional.